| Project/Area Number |
22590899
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Tokai University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
MATSUSAKA Taiji 東海大学, 医学部, 准教授 (50317749)
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| Co-Investigator(Renkei-kenkyūsha) |
ICHIKAWA Iekuni 東海大学, 医学部, 教授 (80317768)
MIYAZAKI Yoichi 東京慈恵会医科大学, 医学部, 講師 (60266690)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 腎臓学 / 腎尿路形成異常 / ポドサイト / 糸球体傷害 / Foxc1 / Foxc2 / 転写因子 / 分化 / 糸球体硬化 |
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| Research Abstract |
This project is aimed to clarify roles of Foxc1 and Foxc2 in the kidney development and the development of glomerular sclerosis. Mice carrying null mutated Foxc1 gene frequently develop anomalous double collecting system due to ectopic budding. However, ectopic budding per se does not contribute to kidney dysplasia. It is intriguing that Foxc1 expression does not affect the fate of metanephric mesenchyme where it is expressed but controls the site of bud formation by the Wolffian duct. We are analyzing kidney tissues from Foxc2 null mice, podocyte specific Foxc1 knockoutmice. We also generated Foxc2 loxP mice that enable us to generate kidney specific Foxc2 conditional knockout mice.
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